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Cathepsin K deficiency aggravates lung injury in hyperoxia-exposed newborn mice




TekijätKnaapi J, Lukkarinen H, Kiviranta R, Vuorio E, Kaapa P

KustantajaINFORMA HEALTHCARE

Julkaisuvuosi2011

JournalExperimental Lung Research

Tietokannassa oleva lehden nimiEXPERIMENTAL LUNG RESEARCH

Lehden akronyymiEXP LUNG RES

Numero sarjassa7

Vuosikerta37

Numero7

Aloitussivu408

Lopetussivu418

Sivujen määrä11

ISSN0190-2148

DOIhttps://doi.org/10.3109/01902148.2011.581738


Tiivistelmä
Cathepsin K (CatK) is a potent collagenase and elastase and may be involved in the development of neonatal bronchopulmonary dysplasia. The authors evaluated the effects of CatK deletion on neonatal lung development and response to prolonged hyperoxic challenge. CatK deficiency resulted in thinner alveolar walls than wild-type littermates on postnatal day (PN) 7. However, no morphological difference could be detected between CatK-deficient and control groups on PN 14. Exposure to 90% oxygen for 7 days after birth caused intensive CatK expression in the bronchial epithelium and alveolar macrophages of wild-type mice. Hyperoxia caused fatal respiratory distress in both groups of mice. However, whereas similar to 20% of wild-type mice survived for 2 weeks in hyperoxia, all CatK-deficient mice died within the first 9 postnatal days. Hyperoxia-exposed lungs of CatK-deficient mice contained high number of macrophages and multinucleated giant cells and had increased content of reduced glutathione, indicating intensified pulmonary oxidative stress. These results suggest that CatK is involved in pulmonary development and it may be an important host-defence protease in the oxygen-stressed newborn lung.



Last updated on 2024-26-11 at 17:32